The age at which alcohol consumption by young adults begins is reported to be ever decreasing. Recent surveys indicate that over 10% of 13- year olds use alcohol and about 70% of high schoolers consume alcohol more than once per month. Of these individuals, nearly one-third report binge drinking (defined as consuming more than 5 drinks per occasion) on a weekly basis. In light of these astonishing statistics, our lack of understanding about the underlying causes of adolescent-onset drinking is surprising as well as disturbing. The largest amount of data on this topic has come from studies using selectively bred strains of rodents showing a clear genetic determinant of alcoholism. However, it is also recognized that genetics alone cannot account for the prevalence of alcohol abuse. Experiential factors must also act, either alone or in concert with genetic predisposition. Due to the early age of onset of alcohol consumption patterns, it is likely that experiences with alcohol occurring early in life contribute to later acceptance of this drug. The long-term objective of the proposed research plan is to understand more fully the mechanisms, behavioral and neurochemical, through which socially mediated increases in ethanol preferences are acquired by preweanling and periadolescent rats. The research will build upon a paradigm recently developed by the PI for rapidly inducing ethanol preferences in preweanling and periadolescent rats. Briefly, one animal (demonstrator) is intragastrically administered a dose of ethanol shortly before a 30-min period of behavioral interaction with the experimental subject (observer). In several experiments we have shown that observers subsequently increase their ethanol intake by up to 75-150% over control levels. Our working hypothesis is that observers detect respired ethanol cues on the breath of the demonstrator in the presence of an endogenous carbon based constituent of rat breath (carbon disulfide), and carbon disulfide promotes the release of endogenous opioids that serve functionally as the reinforcer for the conditioning of preferences for ethanol. To test this hypothesis, we will examine the role of endogenous opioids in promoting the increased ethanol intake patterns through pharmacologically manipulating primarily mu and kappa opioid receptors. The end result of this work will be an increased understanding of the neurochemical and behavioral factors underlying social acquisition of ethanol preferences.